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Infection and Immunity, October 2008, p. 4489-4497, Vol. 76, No. 10
0019-9567/08/$08.00+0     doi:10.1128/IAI.00270-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Human Mast Cell Activation by Staphylococcus aureus: Interleukin-8 and Tumor Necrosis Factor Alpha Release and the Role of Toll-Like Receptor 2 and CD48 Molecules{triangledown}

Claudio M. Rocha-de-Souza,1 Beata Berent-Maoz,1 David Mankuta,2 Allon E. Moses,3 and Francesca Levi-Schaffer1*

Department of Pharmacology and Experimental Therapeutics, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel,1 Department of Obstetrics and Gynecology, Hadassah University Hospital, Jerusalem, Israel,2 Department of Clinical Microbiology and Infectious Diseases, Hadassah University Hospital, Jerusalem, Israel3

Received 27 February 2008/ Returned for modification 17 April 2008/ Accepted 10 July 2008

The ability of Staphylococcus aureus to invade and survive within host cells is believed to contribute to its propensity to cause persistent and metastatic infections. In addition, S. aureus infections often are associated with atopic diseases such as dermatitis, rhinitis, and asthma. Mast cells, the key cells of allergic diseases, have a pivotal role in innate immunity and have the capacity of phagocytosis, and they can destroy some pathogenic bacteria. However, little is known about the ability of some other bacteria to survive and overcome mast cell phagocytosis. Therefore, we were interested in evaluating the interplay between mast cells and S. aureus. In this study, we show that human cord blood-derived mast cells (CBMC) can be infected by pathogenic S. aureus. S. aureus displayed a high adherence to mast cells as well as invasive and survival abilities within them. However, when infections were performed in the presence of cytochalasin D or when CBMC were preincubated with anti-Toll-like receptor 2 (TLR2) or anti-CD48 antibodies, the invasiveness and the inflammatory response were abrogated, respectively. Furthermore, we observed an increase of TLR2 and CD48 molecules on CBMC after S. aureus infection. The infection of CBMC with S. aureus also caused the release of tumor necrosis factor alpha (TNF-{alpha}) and interleukin-8 (IL-8). Both live and killed S. aureus organisms were found to trigger TNF-{alpha} and IL-8 release by CBMC in a time-dependent manner. Cumulatively, these findings suggest that S. aureus internalizes and survives in mast cells. This may play an important role in infections and in atopic diseases associated with S. aureus.

* Corresponding author. Mailing address: Department of Pharmacology and Experimental Therapeutics, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, POB 12065, Jerusalem 91120, Israel. Phone: 972-2-6757512. Fax: 972-2-6758144. E-mail: fls{at}cc.huji.ac.il

{triangledown} Published ahead of print on 21 July 2008.

Editor: B. A. McCormick

Infection and Immunity, October 2008, p. 4489-4497, Vol. 76, No. 10
0019-9567/08/$08.00+0     doi:10.1128/IAI.00270-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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